The rupture of unstable or vulnerable atherosclerotic plaques located on the walls of coronary arteries, the carotid arteries, and other cardiovascular arteries, combined with associated thrombosis, is recognized as a common cause of acute coronary syndrome (ACS) such as unstable angina, myocardial infarction, and sudden ischemic cardiac death. Stabilization or reduction of vulnerable plaques motivates the current medical research in vulnerable plaque detection and treatment.
Vulnerable plaque is formed in the vessels of the heart and those supplying blood to the brain. It largely goes undetected, though its shape and composition make it susceptible to disruption, resulting in a blood clot that can cut the supply of blood to the heart or brain, producing chest pain, heart attack or stroke.
Vulnerable plaques are small lesions typically comprising a lipid-rich core, surrounded by a thin, collagenous cap with varying degrees of smooth muscle cells. The vulnerable plaques form within the walls of cardiovascular vessels, and are often eccentric in shape with irregular borders. The plaques may be characterized by a thickened arterial wall, partial stenosis, and generally elliptical distortion of the cardiovascular lumen with blockages ranging from zero up to about 70%. Stenoses are generally less severe with vulnerable plaques than stable plaques. However, mild stenoses are far more common and are responsible for more occlusions than tighter stenoses. Vulnerable plaques may be differentiated by their size, shape and composition of their lipid cores and fibrous caps. Acute lesions are larger with crescent-shaped cores rich in cholesterol esters with extracellular lipid accumulation. The fibrous cap may be infiltrated with macrophages throughout and at the borders in contact with normal intima, a precursor to a disruption of the vulnerable plaque initiated with mechanical strain or degradation of the wall thickness.
The fibrous cap may fatigue and rupture from mechanical stresses, releasing macrophages and tissue factor leading to thrombosis. Tension within the cap occurs with elevated blood pressure and larger vessel radius. Cyclical tension and compression of the cap occur with normal systolic-diastolic pressure changes that increase with faster heart rate and increased activity. Bodily movements and physical exertion may stress the plaque and exacerbate the onset of fissures in the cap. The cap may also degrade from the secretion of proteolytic enzymes such as plasminogen activators and metalloproteinases from lipid-filled macrophages (foam cells) resulting in plaque disruption and atherogenic vulnerability. The cap may be compromised by the presence of inflammation and swelling. As a result, activated inflammatory cells release heat that, when detected, indicates the presence and progression of vulnerable plaque.
Many devices have been proposed to detect vulnerable plaque. Magnetic resonance imaging, nuclear imaging techniques, endovascular ultrasonography, angiography, angioscopy, infrared spectroscopy, and cardiovascular wall temperature measurements may be used to determine the presence and location of carotid, aortic and coronary atherosclerotic plaques. Included in such devices are thermal sensing catheters, as well as infrared and optical coherence tomography (OCT) catheters.
Measurement of temperature differences between vulnerable plaques and normal vessels provides direct evidence of inflammatory material in the plaque core and thin walls surrounding the core. Normal arterial wall temperatures are relatively constant at about 0.65 degree centigrade above oral temperature; in contrast, the wall temperatures of patients with coronary artery disease of increasing severity have progressively larger deviations between the temperatures of the plaque lesions and the baseline wall, ranging from 0.1 to 0.2 degrees centigrade for stable angina to 1.25 to 2.65 degrees centigrade in those with acute myocardial infarction. Degradation of the cap thickness may further enhance the observable temperature differential, providing further indications of severity and impending peril. Plaque rupture may be predicted by looking for hot spots in arterial walls that are caused by the release of heat from the activated inflammatory cells.
To properly function, a temperature-sensing device often requires that the device be centered within the arterial lumen. Unfortunately, sensors of a device may be offset from the center of the artery and the artery itself may have eccentricity impacting the accuracy of the measurement. A sensor that moves with respect to the wall, such as to be periodically close or far away, may give imprecise temperature measurements, leading to an incorrect assessment of the vulnerable plaque.
Invasive procedures may provide the best opportunity for vulnerable plaque identification and local treatment. Such methods are conveniently used during angioplasty or other surgical procedures when the patient is undergoing intensive procedures involving catheters.
Instrumented catheters provide imagery and sensor information as the guidewire and catheter body are manipulated through the larger arterial vessels in the body. Often catheters are inserted into the femoral artery in the thigh and threaded up a circuitous path into the heart or through the carotid arteries and into the cerebellum. Cardiovascular wall temperatures may be extracted with thermocouple measurements from a suitably equipped guidewire. The thermocouple is tensioned with a graceful kink in the guidewire, providing direct contact with the lumen wall as the guidewire progresses through the vessels. Measurement accuracy is low due to the pulsing flow of blood in the vicinity of the thermocouple, which rapidly diffuses heat generated by the vulnerable plaque. Contact measurements present an intrinsic risk of generating fissures in the plaque wall and liberating its contents, while increasing the risk of thrombogenic responses and the potential for coronary failure.
Temperature measurements of the cardiovascular walls using intravascular, non-contact techniques are a desirable way to avoid undue traction with the vessel wall. Catheter-based apparatus may ascertain the presence and extent of vulnerable plaque, and allow for immediate, localized treatment of the atherosclerotic lesions. While non-contact, catheter-based diagnosis and treatment are attractive therapeutic methodologies for stabilization and abatement of vulnerable plaque, accurate determination of wall temperature is difficult due to the pulsating fluid flow through the vessel and around the temperature sensor. The amount of error in temperature measurement increases as a temperature sensor moves further from the vascular wall. Thermal imaging devices are similarly compromised due to varying opacities of the blood in the vessel. Compensation for errors introduced in the measurement of distance between the temperature sensor and the cardiovascular wall would increase the accuracy of the temperature measurements and provide a more accurate determination of the extent and severity of the vulnerable plaque.
The temperature of the cardiovascular fluid and the cardiovascular wall is affected by the rate of fluid flow in the vessel. Temperature variations due to flow are on the order of several tenths of a degree, and compensation of the temperature measurements with flow measurements would provide a more accurate measurement of cardiovascular wall temperature to determine the presence and progression of the vulnerable plaque. Natural pulsations of the blood within the cardiovascular vessel cause a rise and fall of the measured temperature. Blood flow within the vessel may have a significant effect on the temperature measurement and should be accounted for in temperature measurements.
It is an object of this invention, therefore, to provide a method and system for determining vulnerable plaque and other vascular conditions using improved temperature sensing, to provide an option for local treatment or long-term treatment of the vulnerable plaque, and to overcome the deficiencies and limitations described above.